Sleep Standards and Health Affects

Sleep is terribly important and a lot of people are suffering from sleep disorders of various sorts without knowing it. In diving into the subject of sleep, I realized that physicians and researchers have learned a lot since some 20 years ago when I went in for a sleep study only to be told everything was fine. Back then, sleep labs used a very crude metric to discriminate between those with sleep disordered breathing and those that were considered “normal”.

In the past, patients were wired up to monitoring equipment and then sleep lab technicians looked for two types of events while a person slept. First, they looked to see if the person stopped breathing (apnea). Second, they looked for hypopneas. This is when breathing becames shallow or weak to the degree that blood oxygen levels drop by at least 4%, or the person wakes up – even if it was only momentarily. If the apnea or hypopnea lasted at least 10 seconds, they added it to their score sheet. They also kept track of the total number of hours slept by monitoring brain wavelengths.

After collecting a night of data, the AHI (Apnea Hypopnea Index) was calculated by dividing the total number of apneas and hypopneas longer than 10 seconds by the total number of hours slept to come up with an average. The AHI score was used to determined if you had an issue or not. For example, when the AHI score was over 15 events per hour, then the sleep disorder was considered to be moderate. Sounds pretty straight forward; right?

Well, let’s think about this for a minute. What if you stopped breathing for 4 seconds and then took two good breaths in the next 8 seconds followed by another 4 second apnea and so on and on? Well, your sleep doctor would tell you you’re just fine. So even though you weren’t breathing one-third of the time, because you never crossed the arbitrary 10-second threshold, you’d be given the false impression your sleep was OK! Note: The number of apneas is a bit of an exaggeration but you get my point – under 10 seconds equals no problem.

Now consider a different scenario that is also quite common. In this situation, you continue to breath. However, due to a blockage in your upper airway from excess tissue on your palette, you have great difficulty breathing when your muscles relax during deeper sleep stages This is called Upper Airway Resistance Syndrome (UARS). In effect, you are pulling air in through a straw for hours each night. However, because you’re younger and not overweight, your body is able to keep blood oxygen levels up and you muddle through. Once again, you would be told everything is fine and sent home.

Does any of this make sense? Hell no. Do you think your body isn’t going to notice that it’s not getting enough air? Not a chance. Do you think when this happens night after night and year after year that your sympathetic nervous system isn’t going to get lit up resulting in a whole host of health issues? No way. Do you think that you’re not going to unconsciously recognize that sleep is sort of a scary proposition and consequently not end up having issues like racing thoughts, insomnia, anxiety, and the like? Think again.

Well, here’s the real kicker. In spite of plenty of studies showing just how antiquated the AHI scoring system is, it’s still used today by the insurance industry to determine who will receive coverage. In addition, although sleep labs are required to perform more sophisticated monitoring, many do a very poor job of it. On top of all of this, the bulk of doctors still operate under the false assumption that only overweight men with large neck diameters tend to have sleep disorders. It’s a real travesty that results in millions upon millions being left untreated.

So how much does good sleep really matter? You be the judge. Below is a list of poor sleep related symptoms that I compiled while reading through a couple books and listening to hour after hour of podcasts on the subject. It’s pretty stunning. Further down in this article, you can peruse the notes I took of related podcasts to get a better sense of the impact of sleep disorders.

Excellent Sleep Disorders Video

Symptoms of Sleep Disorders

Depression

Negative Thoughts

Racing Thoughts

Irritability

Feeling Overwhelmed

Anxiety & Fear (anxiety is the #1 complaint)

Lack of Motivation

Chronic Fatigue

Sleepiness (after meals, in afternoon, during long drives, etc.)

Nightmares (important to learn how to work with nightmares)

Waking Up Panicky or Jumpy (adrenaline rush)

Fitful or Fragmented Sleep with Frequent Waking (impossible to gauge without study)

Insomnia (can’t fall or stay asleep) – when sleeping pills don’t work the chances of an insomniac having disordered sleep is 90%. Nearly 100% of Insomniacs that wake in the middle of the night have disordered sleep. Insomniacs diagnosed with a sleep disorder do best on more advanced PAP machines with lower pressures that make the person less anxious.

Bruxism (grinding teeth)

General Pain (especially head, neck, and joints)

Arthritis

Weight Gain

Hypertension (high blood pressure that cannot be resolved)

Heart Problems

Brain Plaque and Tangles Identical to Alzheimer’s

Dry Mouth (especially in morning)

Headaches (especially in morning)

Nocturia (nighttime urination) – trying to pull in air against an obstructed upper airway causes a vacuum in the chest cavity that then stretches the atrial chambers of the heart. This stretching causes the heart to think the body has too much fluid. Consequently, it produces atrial natriuretic peptide (ANP). ANP is a diuretic hormone that causes the person to have night sweats and urinate more in a mistaken effort to get rid of excess fluid.

Do I Have A Sleep Disorder?

So let me guess. You’re probably thinking like I did when a helpful reader, Sean, sent me the very thorough information below and suggested that I take a serious look at sleep disordered breathing. To be truthful, I didn’t really want to hear it. After all, don’t I have enough on my plate already (parasites, hypothyroidism, heavy metals, mold, etc.)? Besides, I’d had a sleep study decades ago and they said I was fine.

Looking over the typical list of risk factors doctors use to determine if a sleep study is warranted below, I didn’t really feel like I fit the mold. I’m not overweight or have a large neck, I’ve had my tonsils out when I was a kid, I kept my wisdom teeth because there was plenty of room, and so on. Granted, I almost always wake up after four hours of sleep for about an hour before going back to bed, however I just figured this was mostly from aches and pains.

Limited Sleep Apnea Risk Factors

Being male

Being overweight

Being over age 40

Having a large neck size (17 inches or greater in men and 16 inches or greater in women)

Having large tonsils, a large tongue, or a small jaw bone – having large tonsils, adenoids, and tongue inside a small mouth is a recipe for sleep disordered breathing.

Having a family history of sleep apnea

GERD/LRPD – Laryngopharyngeal Reflux Disease (LPRD) is when stomach contents flow up into the aero-digestive tract and cause symptoms. Note: Having an upper airway obstruction causes the lungs, airway, and stomach to be put under negative pressure (suction) as a person tries to inhale but can’t. This can draw stomach acid up into the throat. Even though the amount is often very small, it is very damaging. In Sleep Interrupted author Dr. Steven Park writes, “…LRPD is silent, the only symptoms being throat clearing, post-nasal drip, a lump sensation in the throat, hoarseness, cough, coughing, or difficulty swallowing.”

Nasal obstruction due to a deviated septum, allergies, or sinus problems – any doctor can look into your nose and see if the passageways are clear. It’s easy to see a deviated septum and enflamed tissue. If everything looks normal and you can breathe relatively equally out of both nostrils, then chances of having a blockage further down that is only visible with a fiber optic camera is small. Place an index finger on either side of your nose. Push and lift to flare your nostrils. Is your breathing notably better?

However, after digging into this subject deeper, what I learned is that the list above does a poor job in capturing all the folks with sleep disorders. For example, there are lots of skinny women that have severely disturbed sleep. The old rule of thumb that only fat men with large necks that snore is completely wrong. To help round out the list above, below is the list of predictors Dr. Krakow mentioned in his video along with a list I made while studying this subject.

Dr. Kralow’s Sleep Disorder Predictors

Daytime Sleepiness

Snoring Loudly – snoring in general is not a good indicator but snoring loudly is

Mallampati and Friedman Scoring – indicates the degree of airway opening. Sit up, look up to ceiling, open mouth, and stick out your tongue.

Crowded Teeth/ Large Tongue – 70% with a scalloped tongue have sleep disorders

Frenulum Restricted Tongue Movement – can you touch the back of your upper teeth with your tongue when your mouth is wide open? While doing this, can you easily lift the back of your tongue creating a spacious cave all the way back to where the tongue attaches? If you can’t, you may be “tongue tied”.

Nose Breathing Difficulty – Blow out with the nose pinched and mouth shut to observe if any passages tend to block off. Also, you should be able to breath hard through one nostril while pinching the other closed. Finally, flare both nostrils. Does it improve your breathing?

Mouth Breathing and Over-Breathing (see Buteyko breathing) – Mouth breathing can also change the sinus and oral microflora. Maybe this is why I keep getting MARCoNS?

So it turns out I’ve got many of symptoms in Dr. Krakow list. Just as enlightening was learning about facial structure. As mentioned, I’d kept all my wisdom teeth because it was always felt there was plenty of room. However, I’ve since learned that the curvature of the upper and lower rows of my teeth (dental arch) is narrow. Additionally, I have a highly crowned palette with excessive soft tissue, a large and scalloped tongue with a Mallampatti score of 4. To this add a slightly recessed chin, an elongated face, and the tendency to “mouth breath” when stressed. Since digging into this subject, I’ve been paying attention and have noticed that I perpetually tend to hold my mouth slightly open, even though my lips are sealed, in an attempt to open up the back of my throat. Wow, facial structure and mouth breathing are really telling.

The way I figure it, at some point early on in my life, my nasal passages became blocked enough that I started breathing through my mouth. I have pictures when I was a few years old with my mouth gaping open. In addition, being bottle feed to some degree along with being fed large spoonfuls of baby food resulted in my developing an improper, “tongue thrust”, swallowing technique making matters worse. Over time, these facts along with a somewhat unhealthy childhood diet have dramatically altered my face.

My elongated face and slightly recessed chin are hallmarks of a “mouth breather” and are strongly correlated to sleep breathing disorders. A recessed lower jaw, long face, a narrow dental arch, and high palette all point toward having a narrow airway at the back of the throat. If the tongue is larger, or there is excess tissue on the roof of the mouth (palette), then the likelihood of sleep disordered breathing is even greater. When muscles relax during sleep, the large tongue or soft tissue can shift back into the narrower airway closing it off.

It’s really amazing when you look over images showing improper and proper facial development. All I can say is that I hope the parents out there are taking note because if caught early, it’s extraordinary how a child’s facial structure can be corrected so they have the typical Hollywood actor’s strong jaw line. There’s a reason we find a forward thrusting and square jaw attractive. It’s a strong indicator of good health on many levels.

After learning this information, I set up an infrared video camera and taped a lapel microphone right under my nose so I could hear my breathing. I knew that if I was simply micro-breathing all night long, or would just “flame out” over and over again, that the video wouldn’t capture these more subtle, but just as devastating, breathing disorders. Still, I had the equipment lying around so I set it up. Note: I used old equipment so there is a fair amount of buzzing that overlays the audio.

Wow, I was really surprised. It was a real “ah-ha” moment. No wonder I would often wake up with my sympathetic nervous system on alert. No wonder I have to urinate in the middle of the night, have nightmares, fatigue, sleepiness, and so on. Really, although not quite as revelatory as when I first learned about of Chronic Inflammatory Response Syndrome (CIRS), this feels really important.

So OK, hopefully I’ve got you sitting up and paying attention at this point. What’s also instructive is to look at some statistics. In Obstructive Sleep Apnea Is A Common Disorder In The Population, the percent of men and women with sleep apnea caused by an obstruction in the upper airway has increased from 22% in men and 17% in women between 1993 and 2013 to 37% in men and 50% in women between 2008 and 2013. Furthermore, I would argue that those percentages are even higher in those that have been suffering from a chronic illness. I’ll get into that a bit more later.

Of note related to increasing percentages of those suffering from sleep disorders is the comment in Dr. Mack Jones on Neurologic Complications of Sleep Apnea by ENT expert Dr. Steven Park. Dr. Park that much of the sleep disordered breathing is a result of smaller mouth size caused by a poor diet. I’m guessing this is of no surprise to most readers. If you’re interested, the Weston Price Foundation article, Cranial & Dental Impacts on Total Health, is a good read with helpful pictures showing how poor diet impacts facial structure resulting in airway obstructions.

Wrapping this section up, if you just look at the statistics alone and completely set aside risk factors, there is a 50% chance sleep is damaging your health if you’re a woman and a 1-in-3 chance it’s damaging your health if you’re a man. That’s pretty major. On top of this, if a handful of the disordered sleep risk factors in the lists sound familiar, this is even more telling. The bottom line is sleep is a huge issue for many and they’re often unaware of it.

Sleep Jargon

Here is a list of sleep related jargon to make reading the Show Notes from select Dr. Steven Park podcasts below easier. It’s also instructive to read as it begins to give a person a sense for the variety in sleep disorders and paves the way for the up-coming article on sleep disorder testing and treatment.

Arousal – waking from sleep regardless of duration. Often when people with upper airway issues fall into stage 3 or REM sleep and become very relaxed, their breathing becomes obstructed enough to awaken them for a few seconds without knowing. When this happens, they have to progress through lighter stage 1 and stage 2 sleep all over again. This can often result in very little restorative stage 3 and REM sleep.

Awakening – waking from sleep for 15 seconds or more. Normal is no more than 5 to 10 awakenings per night. Some will feel tired after only 5 awakenings.

SDB – sleep disorder breathing.

Apnea – stopping breathing.

Central Apnea – stopping breathing due to the brain not sending out signals. When this happens, the chest and abdomen will stop moving along with the cessation of breathing.

OSA (Obstructed Sleep Apnea) – stopping breathing due to a blockage in the upper airway. When this happens, the chest and abdomen will continue to move but breathing stops.

Hypopnea – When the amount of air being taken in is reduced by 30% or more due to shallow or a lower breath rate for at least 10 seconds and this then either causes the blood oxygen level to drop by 4% (or more), or it results in an arousal or fragmentation of sleep.

Hypoxia – when the blood oxygen concentration drops below 90% for a sustained period of time. This often happens during longer apneas.

AHI (Apnea Hypopnea Index) – this is the total number of central and obstructed sleep apneas plus hypopneas lasting 10 seconds or longer in a night divided by the total number of hours slept. A successful SDB surgery is when AHI is reduced 50% and AHI is less than 20 (not a very compelling standard).

AHI Scoring

None/Minimal: AHI < 5 per hour (no insurance coverage)

Mild: AHI = 5, but < 15 per hour (possible insurance coverage)

Moderate: AHI = 15, but < 30 per hour (insurance coverage)

Severe: AHI = 30 per hour

RERA (Respiratory Effort Related Arousals) – when breathing becomes shallow or labored for 10 seconds or more causing a person to wake up (arousal). Often, the arousal is for only a few seconds but is enough to prevent deep sleep. All sleep labs now score RERA events.

UARS (Upper Airway Resistance Syndrome) – resistance in the upper airway due to anything from a deviated septum, to excessive upper palette tissue, to a tongue that drops back in the throat. Current sleep lab monitoring does not necessarily capture UARS events.

RDI (Respiratory Disturbance Index) – the average number of apneas, hypopneas, and RERAs per hour.

OAT (Oral Appliance Therapy) – a dental appliance (looks like upper and lower retainers hinged together) is used to move the lower jaw outward thereby opening up the back of the throat. Also called Mandibular Advancement Device (MAD).

PSG (Polysomnogram) – a sleep study where airflow, chest and stomach movement, heartbeat, blood oxygen concentration, and others are monitored while a person sleeps. The number of variables monitored depends on the “Type” of the sleep study. There are four Sleep Study Types. A Type 1 PSG is performed in a lab with a technician while the Type 3 PSG often used by insurance companies is done at home with fewer parameters monitored and is much less accurate.

HST (Home Sleep Study) – Insurance companies often will only pay for a Type 3 HST that monitors an insufficient number of variables, is scored using a program (not scored by a person), and consequently is often very inaccurate.

My sleep was atrocious when CIRS was at its worst. What’s interesting to speculate about relates to what Dr. Krakow wrote in A Missing Link: Dr Barry Krakow’s Research on Insomnia and SDB. Specifically, he wrote, “Later, we discovered Series et al’s3 work, which showed that noise-induced fragmentation increased upper airway collapsibility in sleepers who previously had been breathing normally. Since then, we have wondered whether insomnia, PTSD, depression, or other mood and anxiety disorders cause initial sleep fragmentation that over a period of months or years leads to SDB (sleep-disordered breathing) but presents on the surface as insomnia.”

Could it be that CIRS acts just like noise-induced sleep fragmentation leading to permanent sleep disorders? Maybe the enlarged ventricles in the brain and VIP treatment resistance seen in older folks with CIRS are a result of SDB. I guess I’m going to be an n=1 case study. Once I get hooked up with Positive Airway Pressure (PAP) therapy, it’ll be interesting to see if VIP is more helpful and observe the number of symptoms that I’ve heretofore been ascribing to CIRS that simply melt away. I’m hopeful.

Continuing with a bit of speculation, I’ve had sleep issues for a long time. Maybe really early stages of CIRS start with disrupted sleep. Over the long haul, we know poor sleep is very damaging. Perhaps poor sleep opens the gates for CIRS hell. Although very difficult, it would be really interesting to do sleep studies on folks before they acquire CIRS, during CIRS, and post treatment of CIRS. Based upon my own experience, my guess is that their sleep gets progressively worse and then improves with treatment.

If we look at a couple specifics, we know Obstructive Sleep Apnea (OSA) causes the blood-brain-barrier and gut lining to become leaky allowing toxins to enter. Maybe this is the actual mechanism by which mold toxins are able to do so much damage in some of those with CIRS whereas previously, biotoxins weren’t of particular issue. Does CIRS cause OSA or is it the other way around?

So here’s an interesting point. During deep sleep, normally Anti-Diuretic Hormone (ADH) is secreted thereby reducing the need to urinate. However, if you have disrupted sleep, ADH will be low and you will have to get up to use the bathroom – irrespective of whether you have CIRS. On top of this, we’ve also now know that sleep obstructions create a vacuum that stretches the heart that then releases the diuretic hormone atrial natriuretic peptide (ANP). It’s like a “double whammy”.

So here’s where it gets interesting related to CIRS. In Neurotoxicology and Teratology, table 1 tells us that about 60% of those with CIRS will have low ADH even though they have high osmolality – salty blood. These are the CIRS folks that have get up in the night to urinate and have night sweats.

ADH is supposed to be high when a person’s blood is too salty. So why is it low in those with CIRS? I’d be willing to bet that these are the folks with sleep disordered breathing (SDB). Did you have labs for CIRS? If so, was your ADH low?

And finally, Sean wrote in with this a possible link between Ehlers Danlos Syndrome (EDS) and soft upper palette tissue that often leads to obstructed sleep. In effect, he wrote, “I suspect many CIRS patients have UARS but don’t even know it. Particularly given the common co-morbidity with CIRS and Ehlers Danlos Syndrome (EDS) Type 3. I think the incidence of EDS in those with CIRS is even higher than the 50% Dr. Ackerley is noticing. A highly crowned palette, narrow dental arches, and extra flexible tissue in the back of the throat, that cannot resist the pull of narrowing air pressure (Venturi Effect), often equates to UARS. Incidentally, most EDS people are stiffer than everyone by their 30s due to the body promoting inflammation in order to stabilize the joints. So it can be very hard to notice for most.”

In any case, there is a lot of symptom overlap between poor sleep and CIRS. In my humble estimation, if you’ve got CIRS, your chances of have a sleep disorder is even greater than the already high probability for the general population.

Apnea causes a vacuum in the chest cavity that then stretches the atrial chambers of the heart. This stretching causes the heart to think the body has too much fluid. Consequently, it produces atrial natriuretic peptide (ANP). ANP is a diuretic hormone that causes the person to urinate more. This lowers levels of the calming mineral, magnesium. Most patients with apnea have a magnesium and vitamin B1 deficiency.

Nasal breathing produces much more nitrous oxide than mouth breathing (50-200ppb versus 10ppb). Nitrous oxide is beneficial. It is an anti-microbial and dilates blood vessels so you’re able to get more oxygen into the body. Mouth breathing brings in more too much oxygen and also lowers carbon dioxide (CO2) levels resulting in a higher blood pH (more alkaline). As blood alkalinity increases, the red blood cells tend to hang onto the oxygen they’re carrying instead of delivering it to the body’s tissue. This can cause the brain to become over excited due to paradoxical lack of oxygen.

Taking a decongestant like Afrin or using Breath Rite nasal strips can help a person determine if they have nasal congestion either due to inflammation or physical structure. Alternatively, to test for nasal constriction, press your index fingers at the sides of the nostrils and slide them toward the outer corners of the eyes.

Breathing in activates the sympathetic nervous system and breathing out the para-sympathetic nervous system. Hence talking, breathing exercises, singing, and didgeridoo tend to be relaxing because the focus is on breathing out.

Neurologic Complications of Sleep Apnea

Dr. Jones had an Apnea Hypoxia Index (AHI) of 27 – stopped breathing 27 times per hour. Neither CPAP or numerous palette and nasal surgeries relieved his symptoms of feeling like he’d been “run over by a truck”. It’s important to get AHI down to zero while many doctors consider an AHI below 5 to be normal. What’s tolerable depends on the person.

The definition of moderate Obstructive Sleep Apnea (OSA) is stopping breath for at least 10 seconds 15-30 times or more every hour. It’s a completely arbitrary definition. If you stop breathing 300 times an hour for 9 seconds, you do not have OSA. If you micro-breath all night long, you don’t have OSA. If every breath requires Herculean effort, you don’t have OSA. If you don’t have OSA, then insurance will likely not cover treatment.

Dr. Guilleminault at Stanford diagnosed Dr. Jones with UARS. UARS creates negative pressure in the chest. Normal vacuum pressure upon inhaling is 5cm of water. With UARS, it can be anywhere from 10-30cm of water. This chest suction causes an increase of blood flow to the right side of the heart and out the left ventricle into the aorta. Echo cardiograms of those with UARS often show varying degrees of collapse of the right and left heart ventricles during UARS events.

Dr. Jones finally had a tracheotomy that resolved his sleep issues.

Dr. Jones was also considering having a Maxillo-mandibular advancement (Bi-Max or MMA) where they saw off the front portion of the upper and lower jaw in order to lengthen them about 0.5”. This pulls the base of the tongue away from the back of the throat. He decided against it because it hardly ever reduces AHI to zero. Dr. Park says the success rate is between from 80% to high 90% – although success is not measured by having zero AHI. Rather, sleep disorder treatment is considered a “success” when the AHI drops by at least 50% and has a value less than 20. Given that an AHI of even 1 is harmful, that isn’t a particularly useful metric.

Dr. Barbara Phillips from U.W. of Kentucky and former President of the National Sleep Foundation maintains that even an AHI of

Dr. Park: You need an AHI of 5 or more to get insurance coverage. Alternatively, if you have heart disease, diabetes, high blood pressure, a stroke, cancer, or car accidents, you may get insurance coverage.

Sleep apnea can cause peripheral neuropathy, obesity due to surges in cortisol, high blood pressure, diabetes, and myocardium impairment that leads to dementia and Alzheimer’s 60% of the time. It destroys every cell in your body. Heart attacks are common in those with sleep apnea.

In mice with the Alzheimer’s gene, hypoxia caused plaque and tangles in the brain identical to those in Alzheimer’s.

Lacunar Infarcts (tiny strokes) in the brain due to lack of blood flow are often seen in those with OSA using regular MRI.

Sleep labs miss OSA 15-20% of the time. This can happen in about 10% of people that have “alpha rhythms” that are very small (low voltage) immediately upon closing their eyes even though they are still wide awake. This can often be mistaken by lab technicians as first-stage sleep.

UARS was “notoriously” missed in sleep labs as little as 10 years ago. It’s important to use nasal cannula pressure transducer technology during the Polysomnography (sleep study) to measure breathing effort. This technology is now required in sleep labs. Alternatively, they may use EMG Plethysmography or Esophageal Manometry Pressue Test. Unfortunately, even though some labs use this equipment, they may not know how to use the equipment properly or score the results. When UARS events are added to sleep apnea and hypoxia events, the total is often much higher.

As a matter of history, a tracheostomy was the only treatment for OSA before CPAP in 1980.

A 10 year old study showed about 23% of men and 10% of women have some degree of sleep apnea. Today, due to smaller and smaller mouth size, most likely due to diet, means it’s even worse today.

Obstructive Sleep Apnea (OSA) is defined as having 15 apneas for at least 10 seconds every hour. If it’s less than 10 seconds, it doesn’t count. If each apnea lasts 2 minutes, it’s rated the same as someone with 10 second apneas. Even for same duration apneas, blood oxygen levels can vary widely where 97% is normal but may be anywhere from the 80’s to 40’s. Also, some people only have apneas during REM sleep which only occurs in the later half of the night. They may have hundreds of apneas during REM but not qualify for OSA. Typically, most apneas occur in the later one-third of the night.

During apneas, blood oxygen drops, CO2 rises, and then the adrenals start producing epinephrine, nor-epinephrine, and cortisol. This causes you to wake up to Stage 1 sleep or wide awake.

The Walking Dead Sleep-Deprived Zombies

If you have crowding in your mouth, it’s important to expand the mouth as opposed to extracting teeth.

The heart becomes scarred with fibrosis material that can lead to atrial fibrillation. A pig study showed that sleep apnea damage reverses when apnea is treated. Ablation of portions of the heart that involves burning or freezing the portion of the heart that is causing misfiring (atrial fibrillation) should never be done until sleep quality is addressed.

Losing weight can help sleep apnea.

In UARS the airway is narrowed but doesn’t close completely. You have to make a high effort to take in breath. It’s hard to pick out arousals on the electro-encephalogram and connect this with higher breath effort. It’s 10 times harder to score UARS. Centers get paid the same amount so this may be why they don’t want to score UARS. It’s easy to see an apnea with a polysomnogram during a sleep study. The breathing stops and oxygen levels drop. Make sure to check that the center knows what they are doing when it comes to measuring and scoring arousals and breathing effort.

The brain has its own lymphatic system for clearing toxins that drains into neck lymph nodes and then chest lymph nodes. It operates at 7cm of water. When CPAP pressures in excess of 7cm of water are used, inter-cranial hypertension (brain pressure) may develop as the brain’s lymph system can’t drain. This would be an argument for using BI-PAP or other adaptive machines. Some people’s breathing rate is very erratic with CPAP.

Dr. Park mentions that there is a “redundancy” at the soft palette that “flops back” suddenly in a small group of people making it impossible to exhale for about 10-15 seconds (similar to doing the valsalva nose pinching technique only with the mouth open). The person ends up holding their breath until there is relaxation signaled by a “flopping noise” at which point they exhale through the mouth. This is often misinterpreted as a central apnea event – brain temporarily stops sending signals to breathe.

Dr. Park says the Apnea Hypoxia Index (AHI) values are completely worthless and vary widely from sleep lab to sleep lab. Some people can have very high AHI values and be symptom free and visa versa.

You can use the recording feature on CPAP machines to see apnea events. Instead of smooth sine waves, the curve goes flat.

A company called Itamar makes a “WatchPAP” that looks for sleep arousals as they stimulate the autonomic nervous system. It does this by looking at blood flow in a finger.

Yogic breathing exercises can be very helpful because they emphasize relaxing exhalation.

Inter-cranial hypertension can cause shrinkage of ventricles. For folks with CIRS like me with small ventricles, being on CPAP that may increase skull pressure and may not be a good idea.

Sleep Apnea Brain Damage Symptoms

OSA damages the brain. The hippocampus, hippocampus fornix fibers (axons), and mammillary bodies at the base of the brain are all severely damaged resulting in impairment of short term memory transference to long term memory. In addition, the insular cortex is hit hard resulting in increased pain sensitivity and high blood pressure that can’t be controlled (hypertension). The cerebellum (motion control, putting thoughts in order, blood pressure regulation) is also badly damaged. However, because the cerebellum has so many brain cells and can compensate for damage (plastic), this often isn’t as much of an issue.

The areas that are damaged are different between males and females. Also, UARS may very well damage different areas than OSA.

The hippocampus can regenerate to a degree that is helped with exercise and supplements. Folks with sleep apnea sweat profusely in the night and need to supplement minerals. In particular, taking vitamin B1 (Thiamine) and magnesium helps oxygen deprived brain cells recover. Almost all sleep apnea people are low on these two nutrients. It’s important to test for Thiamine and magnesium along with drinking plenty of water.

Proton pump inhibitors for acid reflux stop the production of Thiamine and inhibit the uptake of magnesium.

Obstructive Sleep Apnea (OSA) causes the blood-brain-barrier to become leaky allowing toxins to enter the brain. Maybe this is the actual mechanism by which mold toxins are able to do so much damage in those with CIRS whereas previously, biotoxins weren’t of particular issue. Does CIRS cause OSA or is it the other way around?

Sleep issues often worse for women after menopause.

Exercising the upper airway muscles with the didgeridoo or singing can be very helpful. Talking doesn’t strengthen these muscles. Tongue exercises are also helpful. You need to re-train the processes that activate throat muscles during breathing.

Poor sleep makes a person more reactive because they’re less able to handle stress.

There will always be the exceptional few that can get by with 3-4 hours of sleep. For the rest of us, 90-95% of people, about 8 hours of sleep is needed in order to be healthy.

Those with sleep apnea severely underestimate how little sleep they are getting and how dramatically it is impairing their performance including reduced reaction times. The sleep-deprived are as much of a hazard on the road as a drunk driver! Test Your Reaction Time

It’s imperative to not eat within 3-4 hours of bedtime. You may drink water but no tea or foods of any sort. If you do, stomach acid levels will be high when you lie down and subsequently will be drawn up into the throat. This happens due to the suction created when the airway becomes blocked off. The amount of acid may be microscopic but can still be very damaging. Once in the throat, the acid can go into the sinuses, ears, and lungs. Personally, this may be why my nose is always somewhat inflamed and why I can’t clear MARCoNS.

It’s impossible for your bed partner or you to know how well you’re sleeping. Note: In my late twenties, I used to curl up and take an hour-long nap along a wall I’d just framed on a house out in the middle of frigid Wisconsin winters. I was really sleepy! And yet, if you would have asked me, I would not have listed sleep as an issue.

Poor sleep causes depression. If anti-depressants are taken, they often lead to weight gain that then further exacerbates the problem.

Sean’s Sleep Notes

A very kind reader, Sean, got me pointed in the right directions regarding sleep. Below is part of the conversation we had on the subject.
Greg,

I just reread your Sleep Sanctuary post. Reading this again its clear you likely have already transitioned from Upper Airway Resistance Syndrome (UARS) to Obstructive Sleep Apnea (OSA) which is easier to diagnose. If the choking at night was resolved by using the nasal dilators (one trick used by those with UARS) then you may have already solved your problem. I’m guessing however that you are only managing it better than during the darkest days when it was really bad, but it still exists. (An important relationship) is understanding how sleep breathing issues impact the HPA axis.

Since you don’t fit the profile for OSA, I mainly just wanted to make sure you had not discounted sleep breathing issues entirely. You fit the profile for UARS (physically and symptoms) which presents very differently than OSA and is actually more destructive to the HPA axis. I know you looking into home monitoring but since there is no oxygen desaturation during the night with UARS, home monitoring devices cannot find it.

I included a bunch of links below that transition from basic introduction to the rigorous peer reviewed academic papers. You can get your feet wet with the basic stuff but I wanted you to be able to reference the academic literature too. You seem like an inquisitive fellow 🙂

Once you are familiar with UARS I suggest you read these two interviews to better understand how UARS or even Mild Sleep apnea are related to functional somatic issues or HPA axis issues. Dr. Park interviews both of them too which I left links to if you prefer to listen instead of read.

Knowing you have experienced choking at night and that nasal dilation helps you, I’m certain you are experiencing the things both Dr. Gold and Dr. Krakow are discussing in these articles. Instead of choking over and over all night without waking like a typical obese sleep apnea patient, your neurological system is on high alert trying to keep you from choking. So if you do choke (or even get close to choking) you wake immediately and are ready to fight the person trying to suffocate you. (sweating, heart racing, crazy nightmares, etc.)

Then racing thoughts from your amped up brain chemistry and intense anxiety keep you awake until you collapse again to start the cycle all over. This happens until your adrenals are exhausted, thyroid is overworked, cortisol production fails, everything hurts, you are stuck in a state of constant fatigue, and brain fog but also keyed up. Mold contributes to all of this too but your anatomy is the driving factor in UARS. I just think you could benefit from a closer look at sleep.

I think the older the person and the longer CIRS has gone untreated that the likelihood increases. At a minimum, it would seem to me that having Sleep Disordered Breathing (SDB) makes the impact of CIRS worse and treatment harder.

True. But I guess I was wondering whether SDB (without CIRS) could show similar brain abnormalities to CIRS in the Neuroquant thereby convincing a practitioner that the patient had CIRS when in fact SDB was the only underlying condition.

It’s not possible to say because the sleep studies look at brain “damage” meaning impairment in function while NeurQuant (NQ) for CIRS looks at changes in volume. Does brain damage equal shrunken or enlarged volumes? I don’t know. What we can say is that there is serious overlap in the volumes effected in CIRS and Sleep Disorder Breathing (SDB). For examples, the cortical gray matter, the caudate, the thalamus, the putamen, and frontal cortex.

In terms of my own NQ, I find it telling that NQ shows that my hippocampus is shrunken even though generally it gets a bit larger in CIRS. There is no good explanation for this in terms of my understanding of what Dr. Shoemaker has discussed but it makes perfect sense in terms of SDB.

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